Caries and Early Childhood Caries (ECC) Dental caries is an infectious disease caused by bacteria feeding on fermentable carbohydrates (sugars) and releasing organic acids which lower pH and can demineralize enamel without mediating factors such as fluoride and salivary buffers. In brief, caries is a balance between demineralization and remineralization of the enamel over time. Mutans streptococci (MS) (eg S. mutans and S. sobrinus) and Lactobacilli (LB) have been the bacteria most strongly associated with caries. Saliva contains substances (bicarbonate, phosphate, and peptides) that act as buffers to neutralize these acids. The calcium, phosphate, and fluoride in saliva can remineralize tooth enamel by reversing the demineralization process and depositing minerals back into the decayed area (as fluorapatite) (Featherstone, 2000). Most caries preventive agents are directed at some aspect of this host-substrate-bacteria process, either decreasing the presence of the cariogenic factors (bacteria and carbohydrates) or enhancing the protective factors (fluoride). Although great strides have been made in the past 50 years to reduce caries prevalence and severity, 80% of the disease is confined to 20% of the population (as a Pareto distribution) indicating an inequitable disease burden. Early childhood caries (ECC), which is a form of caries in children under age 6, has previously been called nursing caries, nursing bottle syndrome, baby bottle caries, and baby bottle tooth decay (Ripa, 1988). The maxillary anterior primary teeth, usually at low caries risk, are frequently affected at ECC onset. In 1994, [unreadable]early childhood caries[unreadable] became the preferred term since baby bottle use is not always observed (Serwint et al, 1993; Roberts et al, 1994) and many children with nocturnal bottle feeding habits do not develop ECC (Powell, 1976). Children who are breastfed or use a sweetened pacifier also present with ECC, although the caries pattern differs with pacifier use (Milnes, 1996). ECC, being more inclusive, reflects a more complex etiology (Tinanoff, 1998) since bacteria and diet (fermentable carbohydrates) are necessary but not sufficient conditions to cause ECC. Biologic mechanisms of dental caries in general are fairly well-understood. However, the usual mechanisms may be altered in very young children with newly erupted teeth, new exposure to bacteria, immature immune systems, and feeding and oral hygiene practices different fiom older children and adults (Seow, 1998). The extent of these changes is not well understood. Previous studies found ECC prevalence to vary widely, fiom 1% to 85% depending on diagnostic criteria (Ismail & Sohn, 1999), number of teeth examined, child age, race, ethnicity, socioeconomic status (SES), and fluoride exposure. Reviews of the literature highlight marked differences in definitions (until recently), measurement approaches, and difficulties obtaining a representative sample of preschool children (Milnes, 1996; Kaste et al, 1992). Studies have shown ECC to be a predictor of fhture caries in primary (O[unreadable]Sullivan & Tinanoff, 1996) and permanent teeth (Kaste et al, 1992), depending on ECC case definition. Current recommendations (Ismail, 1998; Dnuy et al, 1999) classify ECC as any lesion, since one lesion in very young children is too many.